国际呼吸杂志
國際呼吸雜誌
국제호흡잡지
INTERNATIONAL JOURNAL OF RESPIRATION
2011年
23期
1792-1795
,共4页
八肽胆囊收缩素%大肠杆菌%感染%急性肺损伤
八肽膽囊收縮素%大腸桿菌%感染%急性肺損傷
팔태담낭수축소%대장간균%감염%급성폐손상
Cholecystokinin-octapeptide%Escherichia coli%Infection%Acute lung injury
目的 探讨八肽胆囊收缩素(CCK-8)对大肠杆菌致急性肺损伤(ALI)大鼠肺水肿及炎症反应的抑制作用.方法 将45只雄性SD大鼠按随机数字表法分为3组,ALI/急性呼吸窘迫综合征(ARDS)组、ALI/ARDS+ CCK-8组和对照组.ALI/ARDS组气管注射大肠杆菌制作ALI/ARDS模型；ALI/ARDS+ CCK-8组于注射大肠杆菌后8h制成ALI/ARDS模型,再静脉注射CCK-8( 60μg/kg).分别于12 h、24 h后检测动脉血气判定氧合指数;24 h后处死大鼠取肺脏,测量肺脏湿/干重比；流式细胞术检测肺组织细胞凋亡率；荧光免疫法检测肺血内皮素1.结果 ALI/ARDS+ CCK-8组与ALI/ARDS组比较,氧合指数明显增高(12 h:312士25 vs 249士37,P＜0.01；24 h:297±39 vs 168±44,P＜0.001),肺脏湿/干重比下降(4.28士0.23 vs 4.87±0.29,P＜0.05),肺泡腔及间质水肿和炎细胞浸润较轻,肺脏细胞凋亡率明显减低,内皮素1的水平降低(P＜0.05).结论 外源性CCK-8能明显抑制ALI/ARDS大鼠肺脏炎症反应,减少肺水肿程度,保护肺血管,提高氧合指数,减轻了ALI/ARDS症状.
目的 探討八肽膽囊收縮素(CCK-8)對大腸桿菌緻急性肺損傷(ALI)大鼠肺水腫及炎癥反應的抑製作用.方法 將45隻雄性SD大鼠按隨機數字錶法分為3組,ALI/急性呼吸窘迫綜閤徵(ARDS)組、ALI/ARDS+ CCK-8組和對照組.ALI/ARDS組氣管註射大腸桿菌製作ALI/ARDS模型；ALI/ARDS+ CCK-8組于註射大腸桿菌後8h製成ALI/ARDS模型,再靜脈註射CCK-8( 60μg/kg).分彆于12 h、24 h後檢測動脈血氣判定氧閤指數;24 h後處死大鼠取肺髒,測量肺髒濕/榦重比；流式細胞術檢測肺組織細胞凋亡率；熒光免疫法檢測肺血內皮素1.結果 ALI/ARDS+ CCK-8組與ALI/ARDS組比較,氧閤指數明顯增高(12 h:312士25 vs 249士37,P＜0.01；24 h:297±39 vs 168±44,P＜0.001),肺髒濕/榦重比下降(4.28士0.23 vs 4.87±0.29,P＜0.05),肺泡腔及間質水腫和炎細胞浸潤較輕,肺髒細胞凋亡率明顯減低,內皮素1的水平降低(P＜0.05).結論 外源性CCK-8能明顯抑製ALI/ARDS大鼠肺髒炎癥反應,減少肺水腫程度,保護肺血管,提高氧閤指數,減輕瞭ALI/ARDS癥狀.
목적 탐토팔태담낭수축소(CCK-8)대대장간균치급성폐손상(ALI)대서폐수종급염증반응적억제작용.방법 장45지웅성SD대서안수궤수자표법분위3조,ALI/급성호흡군박종합정(ARDS)조、ALI/ARDS+ CCK-8조화대조조.ALI/ARDS조기관주사대장간균제작ALI/ARDS모형；ALI/ARDS+ CCK-8조우주사대장간균후8h제성ALI/ARDS모형,재정맥주사CCK-8( 60μg/kg).분별우12 h、24 h후검측동맥혈기판정양합지수;24 h후처사대서취폐장,측량폐장습/간중비；류식세포술검측폐조직세포조망솔；형광면역법검측폐혈내피소1.결과 ALI/ARDS+ CCK-8조여ALI/ARDS조비교,양합지수명현증고(12 h:312사25 vs 249사37,P＜0.01；24 h:297±39 vs 168±44,P＜0.001),폐장습/간중비하강(4.28사0.23 vs 4.87±0.29,P＜0.05),폐포강급간질수종화염세포침윤교경,폐장세포조망솔명현감저,내피소1적수평강저(P＜0.05).결론 외원성CCK-8능명현억제ALI/ARDS대서폐장염증반응,감소폐수종정도,보호폐혈관,제고양합지수,감경료ALI/ARDS증상.
Objective To explore the inhibitive effects and potential mechanisms of CCK-8 on ALI/ARDS of infected rats induced by E.coli injection.Methods Forty-five SD male rats were randomly divided into control group,ALI/ARDS group,and ALI/ARDS+CCK-8 group.ALI/ARDS model was induced in rats by 0.9％ normal saline E.coli injection.The rats of ALI/ARDS+CCK-8 group was injected by CCK-8 (60 μtg · kg-1 ) 8 h after E.coli injection,and the control group rats were injected by 0.9％ normal saline in trachea.12 h and 24 h after E.coli or 0.9％ normal saline intratracheal injection,PaO2/FiO2 was recorded,and at 24 h after injetion lung wet/dry ratio,microscopic examination and apoptosis of lung tissue were examined,and endothelin 1 (ET-1) was detected by radioimmunoassay.Results Compared with those of ALI/ARDS group,the PaO2/FiO2 was significantly higher (12 h:312±25 vs 249±37,P ＜0.01;24 h:297±39 vs 168±44,P ＜0.001),the lung wet/dry ratio was decreased (4.28 ± 0.23 vs 4.87±0.29,P ＜ 0.05),and alveolar edema and interstitial edema and infiltration of inflammatory cells were unconspicuous under microscope.The apoptosis index of lung tissue and were significantly lower compared with ALI/ARDS group (P ＜ 0.05).The ET-1 was significantly decreased in ALI/ARDS + CCK-8 group ( P ＜ 0.05).Conclusions Taken together the findings indicate that CCK-8 can inhibit the inflammatroy reaction of ALI/ARDS in rats pneumonia,relieve lung edema,protect the lung cells,downregulat the ET-1 and reduce the vascular leakage function,and increase PaO2/FiO2.The CCK-8 can better the ALI/ARDS clinical symptom significantly.
